avert malpositions and for those where all precautions are neglected.
Thus, prolonged rest in bed favors pes equinus; the use of crutches
necessitates flexion of the thigh and forced extension of the foot;
locomotion without support tends to displace articulations by
superincumbent weight, causing pes calcaneus, genu-recurvatum.
Finally, compensatory deformities must be averted from sound parts, as
scoliosis from shortening of the atrophied leg, equinus from passive
shortening of the gastrocnemii through flexion of the leg, etc.
ETIOLOGY.—Concerning the etiology proper of infantile paralysis little
definite is known. It is probable, as has been already noticed, that
traumatisms have a much more decided influence than is generally
assigned to them. Leyden particularly insists on this influence, and
on the facility with which a traumatism relatively severe for a young
child may be overlooked, because it would not be recognized as such
for an adult. It must be noticed, however, that children are much more
liable to have the arms wrenched and pulled violently than the lower
extremities; yet in a great majority of cases the lesion is situated
in the lumbar cord.
It has been shown that the myelitis, though so limited transversely,
is often far more diffused in the longitudinal axis of the cord than
might be supposed from the permanent paralyses. This fact corresponds
to the initial generalization of the motor disturbance. It seems
possible that the traumatic irritation, starting from the central
extremity of the insulted nerve, diffuses itself through the cord
until it meets with its point of least resistance, and here excites a
focal myelitis. That this point should most frequently be found in the
lumbar cord would be explained by its relatively less elaborate
development, corresponding to the imperfect growth and function of the
lower extremities.
A second cause of anterior poliomyelitis is, almost certainly, the
presence of some poison circulating in the blood. The frequent
occurrence of the accident in the course of one of the exanthemata is
one indication of this; other indications are found in such cases as
that related by Simon, where three children in one family were
suddenly attacked—two on one day, one, twenty-four hours later.[151]
The same author relates a case of motor paralysis in an adult,
followed by atrophy of left lower extremity, and which occurred during
a fit of indigestion caused by eating mussels.[152] The acute
ascending paralysis of Landry, {1152} with its absence of visible
lesion, has been said to strikingly resemble the effects of poison.
Hydrophobia and tetanus are again examples of the predilection
exhibited by certain poisons for the motor regions of the cord.
[Footnote 151: _Journal de Thérap._, 7, vii., 1880, p. 16. These
children belonged to an American family, but were seen by several
distinguished French physicians.]
[Footnote 152: P. 357.]
The evidence that infectious diseases may constitute the immediate
(apparent) causal antecedent of acute poliomyelitis has led, not
unnaturally, to the theory that all cases of acute infantile paralysis
are due to a specific infecting agent, some as yet unknown member of
the great class of pathogenic bacteria. It may be noticed, however,
that the occurrence of the spinal accidents after the ordinary
infectious diseases, as scarlatina and measles, should as well
indicate that a specific agent proper to itself was at least not
essential to its development.[153]
[Footnote 153: Perhaps the occurrence of diphtheria in the course of
scarlatina and typhoid should indicate a similar lack of real
specificity in the morbid agent of the former disease.]
The influence of exposure to cold, which seems to have been sometimes
demonstrated, must probably be interpreted, as in the case of
rheumatism and pneumonia, as effective by means of some poison
generated in the organism when cutaneous secretion, exhalation, or
circulation has been suddenly checked.
DIAGNOSIS.—The diagnosis of the acute anterior poliomyelitis of
childhood is usually easy, but unexpected difficulties occasionally
arise.
Typical cases are markedly different from typical cases of cerebral
paralysis, but in exceptional cases these differences disappear. This
is shown in the following table:
SPINAL PARALYSIS. | CEREBRAL PARALYSIS.
|
Paraplegic or monoplegic | Hemiplegic, (rule). Monoplegic as
(rule). | residuum of hemiplegia or as
| consequence of solitary tubercle
| (exception).
|
Hemiplegic as residuum from |
paraplegia, or original and |
involving facial nerve (very |
exceptional). |
|
Intelligence free (rule). | Intelligence depressed (rule).
|
Intelligence depressed (when | Intelligence free (exception,
spinal paralysis has affected | especially with solitary tubercle).
imbecile children). |
|
Disposition lively. | Disposition apathetic or cross.
|
Initial convulsion unique; | Convulsions repeated; pyrexia
general symptoms of a few | prolonged several days or weeks
hours' duration (rule). | (rule).
|
Convulsion repeated during two |
to three weeks before |
paralysis; fever a month (rare |
exceptions). |
|
Sensibility intact (rule). | Sensibility intact after initial
| period.
|
Occasional hyperæsthesia |
(exception). |
|
Reflexes cutaneous, and | Reflexes intact.
tenderness lowered or lost |
(rule). |
|
Reflexes preserved when only |
single muscles in groups |
paralyzed. |
|
Associated movements of hand | Associated movements frequently
absent (Seeligmüller). | observed in hand.
|
No rigid contractions of upper | Extensive and rigid contractions of
extremity. | upper extremity very frequent.
|
Atrophy of paralyzed muscles | Atrophy very slight.
and arrested development of |
limb, very marked. |
|
Faradic contractility | Electrical reactions normal.
diminished or lost; |
degenerative galvanic |
reaction. |
Rather singularly, the diagnosis from transverse myelitis is less
liable to error than that from cerebral paralysis:
{1153} ANTERIOR POLIOMYELITIS. | TRANSVERSE MYELITIS.
|
Fever brief or absent. | Persistent fever.
|
Sensibility intact. | Hyperæsthesia, then anæsthesia.
|
Decubitus absent. | Presence decubitus.
|
Reflexes lost. | Reflexes increased.
|
Atrophy of muscles. | Atrophy of muscles sometimes as
| intense.
|
Electrical muscular | Loss of electrical contractility,
contractility lost. | but not proportioned to sensory and
| motor disturbance; less rapidly
| completed.
The diagnosis from hæmatomyelitis is almost impossible, and
practically useless. For if the hemorrhage be severe, the child dies
at once, as in Clifford Albutt's case. If less severe, it excites a
myelitis, and the history becomes identical with that of the disease
we are considering; or if the clot beyond the anterior cornua, it is
identified with a vulgar myelitis of traumatic origin.
Progressive muscular atrophy is extremely rare in childhood, but is
occasionally seen under hereditary influence (Friedreich's disease).
In adult cases confusion is not only easy to make, but often difficult
to avoid, especially with the rare, chronic form of poliomyelitis. The
basis of distinction is as follows:
ANTERIOR POLIOMYELITIS. | PROGRESSIVE MUSCULAR ATROPHY.
|
Onset sudden; maximum of | March very gradual; maximum of
paralysis at the beginning. | disease not attained for years.
|
Faradic contractility lost | Faradic contractility not lost
almost at once. | until atrophy complete.
|
Shortening of limbs and | No arrest of development of limbs.
atrophy of limbs (in infantile |
cases). |
|
Functionally associated | Capricious selection of muscles,
muscles frequently associated | but frequent wasting of these at
in paralysis: hand rarely | eminences.
affected. |
Paralysis from lesion of a peripheric nerve closely imitates anterior
spinal paralysis.[154] It is distinguished by closely following the
distribution of the injured nerve, and, usually, by concomitant
lesions of the sensibility and of cutaneous nutrition.
[Footnote 154: The importance of this fact has been shown in the
section on Pathogeny. (See also quotations from Leyden and remarks on
lesions of peripheric nerves.)]
The pseudo-paralysis sometimes observed in syphilitic children as a
consequence of a gummatous infiltration of the bones at the junction
of the epiphysis and diaphysis[155] might easily be mistaken for a
spinal paralysis. But it is an affection peculiar to the new-born; the
electrical reactions of the paralyzed muscles are intact; careful
examination will show that the movements of the muscles are not
impossible, but restrained by pain; often other syphilitic affections
are present.
[Footnote 155: Parrot, Wagner.]
The diagnosis from diphtheritic paralysis is embarrassed, from the
fact that true anterior poliomyelitis may develop in the course of
diphtheria as of other infectious diseases. The paralysis of the soft
palate, preservation of faradic reaction, absence of atrophy, and the
usually rapid recovery must establish the differentiation.
In spinal paralysis there is loss of the reflexes,[156] and also of
faradic {1154} contractility, both of which are preserved in hysteria.
In hysterical paralysis, also, there is no wasting of the affected
muscles.
[Footnote 156: See Gowers's monograph on “Spinal-Cord Diseases” for an
excellent summary of the spinal reflexes.]
Various diseases of the bony skeleton or articulations may simulate
spinal paralysis. Congenital club-foot, caused by unequal development
of the bones and cuticular surfaces, is to be distinguished from the
paralytic variety by the date of its appearance,[157] by the deformity
of the tarsal bones, and by the extreme difficulty of reduction.
[Footnote 157: Though in some cases paralysis of the muscles of the
foot seems to take place during fœtal life, and a club-foot result
which is both congenital and paralytic.]
Caries of the calcaneum, leading the child to walk on the anterior
part of the foot to avoid pressure on the heel, may leave after
recovery such a retraction of the plantar fascia as to cause a degree
of equinus and varus, with apparent paralysis of the peroneal muscles.
I have seen one such case.
Congenital luxation of the hip may simulate paralysis; indeed, by
Verneuil, it has been attributed to an intra-uterine spinal paralysis.
There is, however, no change in the electrical reactions of the
muscles surrounding the joint.
In coxitis, however, Newton Shaffer[158] has demonstrated a moderate
diminution of faradic contractility in such muscles, and a
corresponding degree of atrophy; and this fact might complicate the
diagnosis of paralysis from arthritis of the hip-joint. Gibney[159]
has called attention to the facility with which this confusion may
arise, and Sayre[160] relates cases of infantile paralysis mistaken
for coxitis.
[Footnote 158: _Archives of Medicine_.]
[Footnote 159: _Am. Journ. Med. Sci._, Oct., 1878.]
[Footnote 160: _Orthopædic Surgery_.]
In a case observed by myself, which had been previously diagnosed as
coxitis, the mistake was all the more interesting as the paralysis
which really existed seemed to have been caused by a meningitis rather
than primary myelitis of the cornua.[161] It thus corresponded to the
meningo-myelitic case related by Leyden.
[Footnote 161: The details of this case are as follows: C. P——, aged
11, ten months previous to consultation suffered from febrile attack,
accompanied by retraction of head, severe pains diffused through body
and intense at nape of neck; unconsciousness for thirty-six hours;
vomiting; no convulsions. Case diagnosed as cerebro-spinal meningitis
by attendant physician. Convalescence in a week, but with pain in
lumbar region of back, predominating on right side, so aggravated by
standing or walking that both acts impossible. Coincidently, pain in
right calf; exquisite tenderness to pressure even from stocking. No
complaint in recumbent position. Child could not get from floor to
bed, nor raise right leg from ground. As pain subsided walking became
possible, but right leg dragged. Chronic twitchings on left side,
face, arm, leg. These symptoms lasted ten or twelve weeks, but at end
of nine weeks patient could walk up stairs. In ten months power of
walking almost recovered, but there remained a certain amount of
lordosis and oscillation of pelvis, which is jarred on the left side
while the right leg is swung forward. Recumbent, all movements
executed equally well on both sides and passive motion of the
hip-joint perfectly free. Circumference of right thigh and leg
diminished from one-half to one inch as compared with the left.
Faradic contractility diminished on the right side in the gluteal
muscles, vastus externus, and rectus, and in the gastrocnemii. The
sacro-lumbalis muscle was, unfortunately, not examined, but from the
lordosis was probably affected. The remaining muscles were intact.
Pain on pressure persisted over right side of second, third, and
fourth lumbar vertebræ. Diagnosis was made of a limited meningeal
exudation, with compression of anterior part of cord or of a portion
of the lumbar and of the sacral plexus.]
Scoliosis, which may be caused by the relatively rare unilateral
paralysis of some of the muscles of the trunk, may also be simulated
by paralysis with shortening of one lower extremity. To compensate the
{1155} shortening, the trunk is bent over on the paralyzed side; hence
a lateral curvature, easily reducible, but easily leading into error.
It would seem easy to distinguish traumatic cases of subluxation of
the humerus from those due to paralysis of the deltoid. Yet sometimes
only the history will serve to establish, and that somewhat
doubtfully, the diagnosis.[162]
[Footnote 162: A child of four was brought to me with a stiffness and
rigidity of the shoulder-joint which could only very partially be
overcome by passive motion, and not at all by voluntary effort. The
mother stated that several months previously the child had, without
apparent cause, become suddenly unable to move the arm. After two
months' delay it was taken to a dispensary, and told that the arm was
out of joint, and had it reset under ether. From this date the
stiffness had gradually developed. The deltoid was atrophied, with
marked diminution of the faradic contractility. Question: Were these
signs merely symptomatic of an arthritis consequent on a dislocation,
or was the latter the result of a spinal paralysis of the deltoid?]
THERAPEUTICS.—The treatment of anterior poliomyelitis embraces two
stages. In the first it is directed against inflammation of the spinal
cord and the paralysis of the muscles; in the second period the spinal
lesion has run its course and the paralysis is considered incurable.
Treatment is then directed to the prevention or palliation of
deformities or toward facilitating the functions of the limb in spite
of them.
These two periods are not, however, rigidly separated from each other
in chronological order. From the very outset it is important to take
certain precautions to prevent deformities, and while palliating these
with orthopædic apparatus it is important for years to continue
treatment of the paralyzed muscles in the hope that at least a remnant
of them may be saved. To abandon the case to the orthopædic
instrument-maker, or to neglect the problem of dynamic mechanics while
applying electricity and studying the progress of fatty degeneration,
are errors greatly to be condemned.
The treatment of the initial stage is necessarily purely symptomatic
for the fever and convulsions, since the diagnosis cannot be made out
until these have subsided.
As soon as the diagnosis is clear, however, certain measures should be
adopted to diminish the hyperæmia of the spinal cord. Dally[163]
recommends the ventral decubitus; almost all modern authorities advise
ice to the spine and ergot internally or subcutaneously. Thus,
Althaus[164] makes hypodermic injections of ergotin in doses of
one-fourth of a grain for a child between one and two years old;
one-third of a grain between three and five; and one half grain from
five to ten; and these doses repeated once or twice daily. The only
objection to this treatment is the degree of local irritation it can
hardly fail to occasion. Hammond, who “affirms ergot to be of great
service, the only medicine capable of cutting short the disease or of
limiting its lesions,” recommends the internal administration of the
fluid extract—ten drops three times a day for infants of six months,
half a drachm for children between one and two years.[165]
[Footnote 163: _Journ. Thérap._, t. viii., 1880.]
[Footnote 164: _On Infantile Paralysis_.]
[Footnote 165: I have elsewhere quoted one case of early recovery
under the use of ice and ergot; or was this a case of temporary
paralysis?]
The belladonna treatment, at one time so warmly praised by
Brown-Séquard, retains to-day few adherents.
Simon advises cutaneous revulsives to divert the circulation to the
{1156} surface; thus, hot-air baths, mustard powder sprinkled on
cotton enveloping the limbs. Ross advises mercurial inunction along
the spine, followed by iodine and blisters. At the same time, iodide
of potassium should be given internally in large doses. The action of
this drug upon inflammations of the nerve-centres seems, within
certain limits, to be indisputable, but its mode of action is
certainly very obscure. Where the lesion can be attributed to a
meningo-myelitis,[166] the iodide may be expected to facilitate the
absorption of the exudation. In these cases it should be continued for
a long time.[167]
[Footnote 166: As in Leyden's first case, and my own.]
[Footnote 167: Binz explains the local action of iodine by an
exudation of leucocytes which follows the dilatation of blood-vessels.
These elements break down the exudation into which they are poured,
and thus facilitate its absorption.]
Electrical treatment may be begun by the end of the first week after
the paralysis. At this stage Erb recommends central galvanization as
an antiphlogistic remedy for the myelitis. For this purpose a large
anode must be placed over the spine at the presumed seat of the
lesion, while the cathode is applied over the abdomen. By a slight
modification of the method the cathode is placed over the paralyzed
muscles. The application is stabile, and, according to Erb, should
last from three to ten minutes; according to Bouchut, several hours
daily. Erb's method is intended exclusively as a sedative to the local
inflammation. When the cathode is placed on the muscles it is hoped
that the descending current, replacing the lost nervous impulses, may
avert the threatening degeneration of the muscle and nerve.
Faradization cannot modify the inflammatory lesions of the cord. As a
means of averting degeneration in completely paralyzed muscles it is
inferior to galvanism, and should not therefore be used in those
muscles which refuse to contract under its stimulus. Its immense
utility, however, is as a stimulus to muscles imperfectly paralyzed,
but liable to degenerate from inaction and to be overborne by their
antagonists. The excitation of contractions in such muscles is a
powerful local gymnastic, helping to maintain nutrition by
artificially-excited function.
For the same purpose, muscles inexcitable to the faradic current
should be, when this is possible, made to contract by the interrupted
galvanic current. After this treatment has been prolonged during
several months, the faradic contractility often returns, and the
current then should be changed (Seguin).
The value of electrical treatment has been very differently estimated.
Erb remarks that “its results are not precisely brilliant.” Roth,
whose testimony perhaps is not above suspicion, since evidently
prejudiced, insists that numerous cases fall into his hands which have
submitted for months to electrical treatment without the slightest
benefit. On the other hand, Duchenne, as is well known, has expressed
almost unbounded confidence in the therapeutic efficacy of
faradization, declaring that it was capable of “creating entire
muscles out of a few fibres.”
The sensitiveness of children to the electrical current, and their
terror at its application, seriously interfere with its persistent
use; as, if the patience of the physician is maintained, that of the
parents is very likely to fail in the presence of the cries and
resistance of the child.
It is very probable that some of the failures of electrical treatment
are {1157} due to the attempt to rely upon it exclusively, instead of
suitably combining both electrical methods with each other and with
other remedial measures. With our present knowledge it is safe to
assert the desirability of persistent electrical treatment during at
least the first two years following the paralysis. The currents must
never be too strong—the faradic, at least, never applied for longer
than ten minutes at a time. The muscles should be relaxed by the
position of the limbs (Sayre). If the muscles continue to waste, and
especially if they become fatty, the electrical response will grow
less and less, and finally cease altogether.[168] In the contrary case
the galvanic contraction will become normal in quality, and the
faradic contractility will return and increase, while the atrophy is
arrested and the muscle regains its bulk and voluntary powers.
Sometimes, as already stated, the latter is regained, while faradic
contractility remains greatly diminished.[169]
[Footnote 168: Passing through three stages: faradic contractility
diminished, galvanic contraction increased; faradic response lost,
galvanic degenerative; absence of contraction to either current.]
[Footnote 169: Sayre (_loc. cit._) has noticed cases in which the
muscle would contract several times under faradism, then refuse to do
so for a day or two. This observation, if valid and not due to unequal
working of the battery, is a most curious one.]
A succedaneum to electricity that is highly prized by some authorities
is strychnia, especially when subcutaneously administered.
Pelione[170] relates the cure of two cases in children of four and
five years, after three and four years' duration of the paralysis, by
strychnia—one-half milligramme daily. None should be given to children
under six months, but over that age one-ninety-sixth of a grain may be
given (Hammond). It should not be given subcutaneously more than two
or three times a week (Seeligmüller).[171]
[Footnote 170: _L'Union médicale_, 1883.]
[Footnote 171: Duchenne relates a case of a paralysis general at the
outset and remaining so for six months. It was then treated by
strychnine for five or six months, and at the end of that time had
become limited to the lower extremities (_Elect. local._, ed. 1861, p.
278).]
The incidental action of electricity in attracting blood to the
paralyzed muscles may be sustained by several other methods.
Among these the external application of heat, either dry or in the
form of hot douches, alternating with cold, is an adjuvant remedy of
real importance. Beard has suggested tubing, malleable to the limbs,
for the conduction of hot water. It is desirable to employ massage
immediately after cessation of the hot applications.
On the value of massage and passive gymnastics opinion is even more
variable than in regard to electricity. Roth, a specialist in
orthopædics, places it at the head of all remedial measures, and
denounces electricity in comparison. Many professional manipulators,
ignorant of medical science, continually claim wonderful triumphs over
regular physicians obtained by means of systematized massage.
Volkmann, on the other hand, dismisses the pretensions of the
Heilgymnastik with considerable contempt, declaring that faradization
is the only method which can really secure exercise to paralyzed
muscles.